To test the hypothesis that energy deficits and intracellular ion derangements may be the cellular basis for intrinsic myocardial dysfunction in rats subjected to severe burn with lactated Ringer's resuscitation (Parkland formula), we examined the energy metabolism, intracellular pH and sodium, and mechanical performance simultaneously in perfused beating hearts from sham burn or burn resuscitated rats (43% TBSA, IIIo scald burn, resuscitated for 24 hours). Intracellular calcium was also measured in the myocyte from the same animal models described above. Burn trauma caused a 46% decrease in left ventricular developed pressure, a 69% decrease in +dP/dt max, and a 72% decrease in -dP/dt max. Intracellular to external standard sodium ratio increased (+58%) from 0.31810.027 to 0.50010.048 (p<0.05), and intracellular calcium increased (+67%) from 266113 nM to 445137 nM (p<0.01). The contractile dysfunction and ionic derangement seen in burn resuscitated heart appears to be independent of intracellular pH and energy metabolism as it presented without significant differences of intracellular pH and energy metabolism between burn resuscitated and sham burn groups even when isoproterenol stimulations were given. Our data suggest that burn trauma-induced cardiac dysfunction is accompanied by increases in intracellular Na+ and Ca2+. Neither energy deficits nor intracellular acidosis are primary mediators of post burn cardiac dysfunction in rats subjected to burn and fluid resuscitation.